Cardiology Flashcards
Main risk factors for AF
Non-modifiable - Age - Male sex Modifiable Anything that increase left atrial pressure - Hypertension - Valvular Heart Disease (esp Mitral stenosis from rheumatic heart disease) - Heart failure - Hypertrophic cardiomyopathy - Hyperthyroidism - Obesity - Dyslipidaemia - OSA - Sedentary behaviour
Pathogenesis of AF
- Left atrial stretch
- Htn/mitral stenosis/heart failure - Genetic
- Inflammation
- Metabolic syndrome
Cardioversion in AF time parameters
- Urgent cardioversion
- Only in extreme - <48 hours
- Echo/TFT’s/Renal function
- Anticoagulation, if appropriate with CHADS VASC - > 48 hours or unsure
- TOE essential then anticoagulate for 6 weeks
- Anticoagulate 4-6 weeks then revert
Note no demonstrable different risk in stroke between electro/chemical cardioversion
Adverse effects of amiodarone
- Thyroid toxicity (10%)
- Pulmonary toxicity (1-17%)
- Hepatic toxicity
- Occular toxicity
Main concern with flecainide
Precipitate Atrial flutter with 1:1 conduction
Always prescribe with Beta-Blocker or Non-dihydroperidine CCB (if unable to take BB)
AF rate control what rate should you aim for?
<110
Nb increasing risk with the addition of each rate control agent of her block and PPM requirement.
Which subset of the AF population are considered to get the most benefit from ablation therapy?
Patients with heart failure in whom there is a reasonable expectation of reversion (i.e. not those with well established AF).
Reduced composite endpoint of all cause mortality and unplanned hospitalisation for heart failure
In the general population it is a symptomatic treatment only. Patients need to continue anticoagulation after ablation.
Mainstay of treatment for Atrial Flutter
Anticoagulation
Ablation. Successful in 90% of patients
DO NOT USE FLECAINIDE ALONE.
Atrial flutter ECG findings
Downward p waves in II/III and AVF
Brugada findings on ECG
Downsloping septal ST segment on AVR, V1, V2
Most significant benefit of NOACS over Warfarin in patients with Non-Valvular AF
Reduction in intracerebral haemorrhage
When to use warfarin instead of a DOAC
1) Mechanical heart valve
2) Mitral stenosis and AF
3) CrCL <15
Treatment for patients with VT + structural heart disease
Defibrillator
Which drug is shown to reduce VT and prevent SCD post AMI?
Beta Blockers
Indication for AICD post AMI?
LVEF <35% greater than 40 days post AMI
Indication for AICD for non-ischaemic cardiomyopathy?
QRS >120ms
HF with EF <35% (benefit greatest is ischaemic)
HOCM inheritance pattern
Autosomal Dominant
Most sensitive test in HOCM
ECG
- T wave inversion in II/III/V4/V5/V6
Most common genetic finding in HOCM
Genes that encode sarcomere proteins - most commonly the cardiac B-myosin heavy chain.
Most common genetic finding in ARVC
Mutations in genes encoding Desmosomal proteins
Long QT syndrome genetics
Autosomal Dominant
80% have abnormal QT findings LQT1/2/3
One cardiac conditions where genetics are considered part of the diagnostic criteria.
Management of patients with long QT syndrome
No VT: Beta-Blocker
VT: Beta-Blocker and AICD
In patients with heart failure what is the preferred method of pacing?
Bi ventricular pacemaker
RV pacemaker is associated with increase in heart failure and mortality
Treatment for ARVC and HOCM
AICD
What did the Courage trial show in regards to stable angina
No improvement in outcomes in stable coronary artery disease with PCI. Use optimal medical therapy only (BP lowering therapy, statin, anti-platelet.
Confirmed by the ischaemia trial and orbita study.
Treatment for exertional stable angina (not complete)
1) Aspirin
2) Beta-blocker
3) CCB
4) Nitrates
5) Smoking cessation
6) BP control
7) Diabetes control
8) Weight control
Findings of the Orbita study (PCI vs sham PCI in stable coronary artery disease)
PCI in stable angina (Single vessel disease on good medical therapy)
- Does not improve angina symptoms (increment of exercise time)
What did the Promise trial show?
Established CTCA as a viable alternative to stress testing
- No superior to stress testing but viable alternative
- Reduces the number of normal angiograms done
What does the coronary calcium score stratify for?
Identifies those at risk of an AMI in those with low/intermediate risk factors
Agatson score 0 = highly unlikely to have a cardiovascular event
What did the SCOT-Heart trial establish
CTA associated with decreased mortality when compared with standard care.
Meaning imaging evidence of atheroma = commence statin = better outcome
MOA of PCSK9 (Aliorcumab/Evolocumab)
MAB that binds to PCSK9 and prevents it from internalising the LDL receptor in the liver which is responsible for the metabolism of LDL.
Leads to decreased LDL and decrease myocardial infarction/stroke/coronary revascularisition but no death from any cause or CV death.
Established by the Odyssey/Osler trial - LDL decreased significantly by the PCSK9.
Adverse effects: ? neurocognitive effects
Effect of Icosapent Ethyl effect
1) Lowering triglycerides
2) Decrease CV death/MI/stroke/coronary revascularisation/unstable angina.
FFR coronary lesion functionally significant
- 75: Defer study
- 80: Fame study
Adenosine used to induce maximal hyperaemia
Which access point is better for risk of death in ACS radial or femoral?
Radial artery access (stat sign difference in mortality)
Which second antiplatlet (in addition to aspirin) shows decreased adverse outcomes in ACS
Ticagrelor (and prasugrel but now withdraw from the market - although prasugrel increase bleeding)
Mechanism of ticagrelor-mediated dyspnoea and ventricular pauses?
Adenosine build up
MOA of ticargelor/prausagrel?
Act on the P2Y12 ADP receptor
- ticagrelor binds reveribly
- prasugrel bidn irreversibly (pro drug needs to be matabolised in the liver)
What is aspiration during PCI associated with?
Increased risk of stroke
Therefore routine thrombectomy not indicated
Should you only treat the culprit lesion during STEMI treatment?
No, unless shocked.
Patients with shock - culprit lesion only should be fixed (Culprit-shock trial)
Is PCI or CABG better for 3 Vessel Disease or Left Main Disease?
CABG > PCI if intermediate to high syntax score or diabetic
- Mortality benefit in intermediate and higher syntax scores
- No mortality benefit in lower syntax score
- Mortality benefit in diabetic patients (Freedom trial)
What is the syntax score?
Measure of complexity of multi vessel coronary disease based upon the coronary angiogram findings
In patients with multi vessel disease with diabetes what treatment should be offered
CABG
In which patient population could you use mutlivessel PCI for multi vessel disease?
Non-diabetics with a low syntax score on angiography.
In left main disease is PCI inferior to CABG?
Controversial
- Excel: no
- Nobel study: yes
Does inflammation play a role in atherosclerosis?
Yes , associated with CRP
Confirmed by Cantos trial (Canukinumab)
Should patients with no cardvioscular risk take aspirin as primary prevention?
No - aspree trial established increases all cause mortality due to bleeding.
Indication for primary prevention with PCSK9 inhibitors in Australia
1) Homozygous familial hypercholesterolaemia (LDL >2.6 PBS)
2) Heterozygous familial hypercholesterolaemia with risk enhancers (LPA>50/Coronary calcium score >100, ATSI, atherosclerosis, angia) and LDL >3.3 (>2.6 PBS)
3) Heterozygous familal hypercholesterolaemia without risk enhancers and LDL >4.5 (>5 PBS)
Nb for PBS requirements must have been on a statin for at least 12 weeks
Indication for secondary prevention with PCSK9 inhibitors in Australia
1) Acute coronary syndrome with risk enhancers and LDL >1.8 (PBS >2.6)
2) Acute coronary syndrome without risk enhancers and LDL >2.6
Nb for PBS requirements must have been on a statin for at least 12 weeks
Indications for balloon valvuloplasty in mitral stenosis
1) Symptomatic i.e. progressive dyspnoea (NYHA II-IV)
2) Mitral valve area <1.5cm squared
3) Assymptomatic + thromboembolism or paroxysmal AF or significant pulmonary hypertension (PAP >50mmhg)
Contraindications to balloon valvulopasty for mitral stenosis
1) Left atrial thrombus
2) Fused commissures
3) Severe mitral regurgitation
4) Severe concomitant valvular or CAD
Echo criteria for severe AS
1) Valve area <1cm squared
2) Indexed valve area <0.6cm/m squared
3) Mean gradient >40mmHg
4) Maximum jet velocity >4.0 m/second
5) Velocity ratio <0.25
Indications for TAVI
1) Severe AS where surgical AVR is too high risk \+ 2) Life expectancy > 1 year \+ 3) Likely to have symptomatic benefit
Contraindications to TAVI
1) Heart team doesn’t agree
2) Unsuitable anatomy
3) Endocarditis
4) LV thrombus
5) Other symptoms likely to remain symptomatic even with TAVI i.e severe COPD/ severe pulmonary hypertension
6) Life expectancy <1 year
Indications for surgical intervention for Aortic Regurgitation
1) Sever symptomatic
2) Assymptomatic and LVEF <50%
3) Having CAGS/other aortic surgery
Indications in Marfan’s patient for intervention on ascending aortic aneurysm
1) Ascending aorta >50mm
2) Ascending aorta >45 mm with risk factors ie family history of rupture
Indications in Non-Marfan’s patient for intervention on ascending aortic aneurysm
1) Ascending aorta >50mm with risk factors
2) All >55mm
Indication for intervention in ASD
1) >10mm
2) Shunt ration >1.5
Treatment for native valve endocarditis
benzylpenicillin 1.8 g (child: 50 mg/kg up to 1.8 g) intravenously, 4-hourly (or ampicillin)
PLUS
flucloxacillin 2 g (child: 50 mg/kg up to 2 g) intravenously, 4-hourly
PLUS
gentamicin intravenously
Treatment for prosthetic valve endocarditis
flucloxacillin 2 g
PLUS
vancomycin
PLUS
gentamicin
Note consider rifampicin
Commonest causative organism for infective endocarditis
Staphylococcus aureus
Indications for surgery in Infective Endocarditis
1) Heart failure
- emergent for refractory pulmonary oedema
- urgent for severe regurgitation and clinical CCF
2) Uncontrolled infection (not just ongoing fever)
Major criteria for IE
1) >2 positive blood cultures with known causative organism
2) 1 positive coxiella culture
3) Imaging evidence on echo or PET/SPECT for prosthetic valve
Minor criteria for IE
1) Fever > 38 degrees
2) Clinical suspicion
3) Embolic phenomena
4) Immunologic phenomena
5) Micro not meeting major criteria
Clinical criteria for diagnosis of IE
1) 2 Major criteria or 2) 1 major criteria and 3 minor criteria or 3) Five minor criteria
Which imaging modality to do after echo to investigate infective endocarditis of prosthetic valve
1) PET/Leukocyte labelled SPECT
Treatment for streptococcal pharyngitis
benzathine benzylpenicillin
or
phenoxymethylpenicillin
Long acting compared to benzyl
Major criteria for Rheumatic Fever in high risk individuals
1) carditis (including subclinical echocardiograph changes)
2) polyarthritis, aseptic monoarthritis, or polyarthralgia
3) chorea
4) erythema marginatum
5) subcutaneous nodules
Minor criteria for Rheumatic Fever in high risk individuals
1) monoarthralgia
2) fever of 38°C or higher
3) ESR 30 mm/hour or more, or CRP 30 mg/L or more
prolonged PR interval on ECG
Diagnosis of initial episode of rheumatic fever
Evidence of preceding Strep Pyogenes infection (Anti-streptolysin antibody or Anti-DNase B titres
1) two major,
or
2) one major plus two minor, manifestations
Diagnosis of recurrent episode of rheumatic fever
Evidence of preceding Strep Pyogenes infection 1) two major, or 2) one major plus one minor or 3) three minor, manifestations
Treatment for patent ductus arteriosus
Duct closure (due to risk of endocarditis) Completed percutaneously in adults
Indications for treatment of aortic coarctation
1) Hypertension
2) Gradient of 40mmHg (between proximal and distal)
Treatment for severe MS during pregnancy
1) Bed rest
2) Beta Blocker - avoid atenolol as assocaited with low birth weight
3) Baloon valvuloplasty can be completed post 20 weeks (after period of organogenesis)
Treatment for non stable patient with obstructive valve thrombosis
1) tertiary centre - surgery
2) peripheral site - thrombolysis
Treatment for stable patient with obstructive valve thrombosis
Heparin and aspirin
Treatment for stable patient with non-obstructive valve thrombosis
Non embolic event: optimise anti-coagulation
Embolic event: surgery
Indications for IE prophylaxis prior to dental procedures
1) Prosthetic valve (including TAVI)
2) Previous episode of IE
3) Patients with congenital heart disease that is cyanotic or has been repaired using prosthetic materials
Ampicllin/Amoxicillin or Clindamycin 30-60 minutes prior to the procedure.
Echocardiography finding in constrictive pericarditis
Pericardial thickening
Interventricular septal shift during respiration (toward the left ventricle)
Respiratory variation in filling of left and right ventricles.
Plethora of inferior vena cava
Definitive treatment of constrictive pericarditis with heart failure
Pericardiectomy
Most frequent malignant cause of cardiac tamponade
Breast
Lung
Clinical findings of cardiac tamponade
1) Tachycardia (compensatory)
2) Pulsus paradoxus (a drop of >10mmHg systolic during inspiration)
3) Elevated JVP
4) Hypotension
ECG findings in cardiac tamponade
1) Electrical alternans
2) Tachycardia
Echo findings in cardiac tamponade
1) Diastolic right atrium and ventricular collapse
2) Ventricular septal shifting with respiration
3) Enlargement of the inferior vena cava
Management of cardiac tamponade
1) IVF to stabilise hypotension (even if signs of failure)
2) Pericardiocentesis
Medications that can be used to slow the progression of aortic disease in Marfan’s syndrome
1) Beta Blocker
2) Lorsartan
In bicuspid aorta at what size of aortic aneurysm do you commence annual echocardiographic assessment?
4.0-4.5cm aortic root or aortic dimension
In patients with Marfan syndrome how frequently should you monitor the aortic dimension
1) 6 months after diagnosis
2) Annually thereafter if aortic dimension <4.5cm
3) More frequently if aortic dimension >4.5cm
Indication for elective aortic repair (Marfan and non-marfan) - incomplete
1) Marfan
> 5.0com
2) Non-Marfan
Indications for statins
1) Individuals aged 40-75 with cardiovascular risk >7.5%
2) Individuals with history of cardiovascular event
3) Aged >21 with LDL >4.9
4) People with diabetes
Treatment for hypertriglycerideaemia
Statin
Beta-blockers indicated in hear failure reduced ejection fraction LVEF <40%
1) bisoprolol
2) carvedilol
3) controlled or extended release metoprolol
4) nebivolol
Criteria for prolonged QT in men and women
Men: > 440
Women >460
Mitral valve stenosis indications for repair
not complete
Repair > Replacement
> Left ventricular end diastolic dimension > 40mm
> Symptomatic
If unable to do surgical replacement then transcatheter
Medication for mechanical valve
Warfarin + Aspirin
Drug with greatest mortality benefit in HF
Beta Blocker
ARNI in Heart Failure
LVEF <40% and failure on ACE/ARB
Note need 36 hour washout period
What is pulses paradoxus
Fall of 10mm of SBP on inspiration
Treatment of pericarditis
1) Colchicine
2) NSAID’s
Beta Blockers with mortality benefit in HeRef
1) Bisoprolol
2) Metoprolol Succinate (Long acting)
3) Carvidelol
4) Nebivolol
Key echo feature differentiating between constrictive and restrictive pericarditis
Constrictive pericarditis has ventricular interdepenence on ECHO
Other features
- Right atrial pressure increases both
- Low voltage ECG in both
- E’ - low in restrictive cardiomyopathy and high in constrictive cardiomyopathy
When should non-culprit lesions in STEMI be stented if significant (>75% occlusion or >50% with FFR <80)
Prior to discharge
When does stent restenosis characteristically occur?
3 to 12 months after stent placement. Typically presents with anginal symptoms
Which genetic abnormality is associated with Coarctation of the Aorta
Turners.
All women found to have Coarctation should undergo karyotyping for turners syndrome (45,X, or 45,X0,)
Formula for PVR
(PA-PCWP)/Qp
Indications for biventricular pacing
- Ejection fraction of less than 35%
- left bundle branch block
- QRS greater than 150 ms
- sinus rhythm
- NYHA class 2-4 on maximum medical therapy
Indications for defibrillator placement in hear failure
- ischaemic or non ischaemic cardiomyopathy,
- EF has to be less than 35%
- NYHA class 2-3 symptoms
- survival greater than 1 year.
Mechanism of action of Tirofiban
Gp2b3a inhibitors
In symptomatic AS what is associated with the presence of what clinical feature increases mortality the most?
Heart Failure
Patients with symptomatic severe AS have an average life expectancy of 5, 3 and 2 years with the presence of angina, syncope and heart failure respectively.
Which congenital arrhythmia is associated with a gain of function of sodium channels
LQT3
LQT3 treatment
Mexiletine
Definition of wide complex tachycardia
> 110msec
>3 small boxes
Differential for wide complex tachycardia
Ventricular Tachycardia
SVT with aberrancy or bundle branch block
Paced
Pre-excited tachycardia (integrate A–> V conduction)
Risk factors for VT
Do they have scar?
- Previous myocardial infarction
- Dilated CM
ECG suggestions of VT
Fusion Beats Capture beats Narrower QRS in tachycardia than in SR Notching of S wave q waves North west axis
Primary Prevention indication for ICD
1) Prior MI (40 days ago at least) and LVEF <30%
2) Cardiomyopathy and NYHA 2-4 with LVEF <35%. Note non-ischaemic should have optimal medical therapy for at least 3 months
3) Congenital Long QT syndrome with syncope or VT
4) Hypertrophic Cardiomyopathy or ARVC
5) High-risk patients with Brugada syndrome, catecholaminergic polymorphic VT, and other channelopathies
6) Short QT syndrome
Secondary prevention indication for ICD08
1) Life threatening VT /VF not caused by reversible cause
2) Patients with episodes of spontaneous sustained VT (>30 seconds) in the presence of heart disease
Brugada Syndrome characteristic findings
1) Coved ST segment in V1-V3
2) More common in men and those of Asian descent
3) Arrythmic events often occur at night during sleep
Treatment for Brugada Syndrome
1) ICD
2) Recurrent VT/ICD shocks: quinine therapy
Genetics of Brugada Syndrome
1) Loss of function mutation of SCN5A (sodium channel)
2) SC10A
Types of congenital Long QT syndrome (QT >440msec)
Type 1: Mutation of KCNQ1 encoding a loss of function of potassium channel. Often precipitated by exercise (especially swimming)
Type 2: Mutation of KCHN2 encoding a loss of function of potassium channel. Often precipitated by emotional stimuli, auditory signals ie telephone/alarm clock ringing or sleep
Type 3: Due to mutation of SCN5a encoding a gain of function of sodium channel.
https://images.app.goo.gl/6mLszyDnzJfKoBWj7
Treatment for congenital long QTS
Pharmacological
- Beta Blockade: propanolol or nadolol for patients with syncope/seizures/resuscitated SCA
- Type 3: Mexiletine
Non pharmacological
- For Type 1: Avoidance of swimming and competitive athletics should be considered.
- Left cardiac sympathetic denervation
- ICD in patients with SCA, recurrent arrhythmia despite beta blockade or in men with QTC >550msec or post pubertal women QTC >500msec
Aim of LDL
ETG
Primary prevention: LDL <2.0
Secondary prevention : LDL <1.8
Note European Heart Journal states to aim for LDL <1.4 in patients with established CAD
Familail hypercholesterolaemia
Incidence of 1:250
Autosomal Dominant
Diagnosed via the dutch lipid clinic score (family history, clinical history, physical examination, biochemical results and molecular genetic testing).
Dutch Lipid Score for familial hypercholesterolaemia
> 8: Definite FH
6-8: Probable FH
3-5: Possible FH
0-2: Unlikely FH
Dutch Lipid Score for familial hypercholesterolaemia
> 8: Definite FH
6-8: Probable FH
3-5: Possible FH
0-2: Unlikely FH
Mechanism of action of PCSK9 inhibitors
Bind to PCSK9 and inhibits its activity increasing LDL clearance from the blood.
Note PCSK9 is a pro protein that degrades LDL receptors in the liver. Thereby reducing the ability for hepatocytes to clear LDL from the plasma
Targets for non LDL lipids
Cholesterol <4.0
Non HDL: <2.5
Triglycerides: <2.0
HDL: >1.0
Primary prevention indications for PCSK9 Inhibitors
1) Homozygous FH with LDL >2.6
2) Heterozygous FH with risk enhances such and LDL >3.3mmol/L after 6 weeks of statin therapy + followed by ezetimibe for 6 weeks
3) Heterozygous FH with no risk enhancers and LDL >4.5mmol/L after 6 weeks of maximal statin + followed by 6 weeks of ezetimibe
Note PBS criteria are slightly different
Secondary prevention indications for PCSK9 inhibitors
1) ACS with risk enhances: LDL-C >1.8mmol/L following 6 weeks of maximal statin + 6 weeks of ezetimibe
2) ACS with LDL >2.6mmol/L after 6 weeks of maximal statin + 6 weeks of ezetimibe
